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[家兔脑室内注射组胺后肺动脉压的变化]

[Alterations of pulmonary arterial pressure following intraventricular injection of histamine in rabbits].

作者信息

Wang Y H, Ni H

机构信息

Department of Physiology, Nanjing Medical College.

出版信息

Sheng Li Xue Bao. 1992 Jun;44(3):295-302.

PMID:1455262
Abstract

The changes of the pulmonary arterial pressure (PAP) following microinjection of histamine (HA) into the lateral ventricle in the rabbit were investigated. It was found that (1) Intraventricular injection of HA (50 micrograms) induced either an increase (in the majority) or a decrease in PAP and cardiac output (CO), or a biphasic response characterized by a decrease followed by an increase. Slowing down of heart rate (HR) and elevation of carotid arterial pressure (CAP) were observed accordingly. (2) After bilateral cervical vagotomy or fixing the heart rate by cardiac pacing, drop in CO and PAP in response to HA was no longer observed. Instead, they even showed some constant increase. The pressor response of PAP and CAP to HA could be partially blocked by phentolamine applied intravenously without affecting the increment of CO. On the other hand, intravenous injection of propranolol could totally block the HA-induced increment of CO, but not affect the pressor responses of PAP and CAP. Intravenous injection of hexamethonium or combined application of phentolamine and propranolol could completely abolish all the increment responses in CO, PAP and CAP to HA. (3) The cardiovascular responses to HA could be blocked by the H1 receptor blocker-chlorpheniramine, but not by H2 receptor blocker-cimetidine. It is thus assumed that HA applied intraventricularly can activate the central H1 receptor, thus inducing an increase in the cardiac output and vasoconstriction of pulmonary and peripheral vessels giving rise to an elevation of both PAP and CAP by way of sympathetic nerve. Central application of HA also induces bradycardia by activating vagus nerve.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

研究了向家兔侧脑室内微量注射组胺(HA)后肺动脉压(PAP)的变化。结果发现:(1)脑室内注射HA(50微克)可导致PAP和心输出量(CO)增加(多数情况)或减少,或出现先减少后增加的双相反应。相应地观察到心率(HR)减慢和颈动脉压(CAP)升高。(2)双侧颈迷走神经切断或通过心脏起搏固定心率后,不再观察到HA引起的CO和PAP下降。相反,它们甚至出现一定程度的升高。静脉注射酚妥拉明可部分阻断PAP和CAP对HA的升压反应,但不影响CO的增加。另一方面,静脉注射普萘洛尔可完全阻断HA引起的CO增加,但不影响PAP和CAP的升压反应。静脉注射六甲铵或联合应用酚妥拉明和普萘洛尔可完全消除CO、PAP和CAP对HA的所有增加反应。(3)心血管对HA的反应可被H1受体阻滞剂氯苯那敏阻断,但不能被H2受体阻滞剂西咪替丁阻断。因此推测,脑室内注射HA可激活中枢H1受体,从而通过交感神经引起心输出量增加以及肺血管和外周血管收缩,导致PAP和CAP升高。中枢应用HA还可通过激活迷走神经引起心动过缓。(摘要截短于250字)

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